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Structural Plasticity Analysis of Drosophila Sleep Circuit After Thermogenetic Sleep Deprivation
Author(s) -
Velazquez Yoheilly,
Dubowy Christine,
Sehgal Amita
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.lb538
Subject(s) - sleep (system call) , neuroscience , immunostaining , sleep deprivation , biology , biological neural network , neuroplasticity , structural plasticity , synaptic plasticity , drosophila (subgenus) , circadian rhythm , immunohistochemistry , gene , genetics , receptor , computer science , immunology , operating system
Sleep rebound is a homeostatic process characterized by an increase in sleep drive after sleep deprivation. Previous studies have identified neural circuits in Drosophila implicated in sleep regulation, but whether or not there are structural plasticity changes in these circuits after sleep deprivation, and if there is synaptic connectivity between them is unknown. To answer these questions, we used fluorescent markers to identify neural structural changes following thermogenetic sleep deprivation and further characterize the anatomy of two populations of neurons localized in sleep control regions, ExFl2 neurons and c584‐expressing neurons. Immunostaining of ExFl2 neurons produced strong signals in the fan‐shaped body (FSB) and superior medial protocerebrum, while immunostaining of c584‐expressing neurons produced diffused signals throughout the brain. Total fluorescence of ExFl2 neurons in the FSB showed no difference between the sleep‐deprived group and control. In addition, after developing a protocol for sophisticated analysis of 3D structures of interest, results showed no difference between the groups. Altogether, these results suggest that thermogenetic sleep deprivation does not induce plasticity changes in ExFl2 neurons or c584‐expressing neurons. For future directions, using the same approach in other populations of cells that have been related to sleep, and studying the mechanisms underlying any observed structural plasticity will help to better understand sleep control. Support or Funding Information National Heart, Lung, and Blood Institute (NHLBI) NIH (Grant #5R25HL084665), Biomedical Graduate Studies (BGS), PRISE Program (Grant #R25GM096955) This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .